BACKGROUND: Atherosclerotic cardiovascular disease (ACVD) is worsened by chronic inflammatory diseases. Interleukin receptor antagonists (IL-RAs) and tumour necrosis factor-alpha (TNF) inhibitors have been studied to see if they can prevent cardiovascular events. OBJECTIVES: The purpose of this study was to assess the clinical benefits and harms of IL-RAs and TNF inhibitors in the primary and secondary prevention of ACVD. SEARCH METHODS: The Cochrane Heart Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), Ovid MEDLINE (including In-Process & Other Non-Indexed Citations), Ovid Embase, EBSCO CINAHL plus, and clinical trial registries for ongoing and unpublished studies were searched in February 2024. The reference lists of relevant studies, reviews, meta-analyses and health technology reports were searched to identify additional studies. No limitations on language, date of publication or study type were set. SELECTION CRITERIA: RCTs that recruited people with and without pre-existing ACVD, comparing IL-RAs or TNF inhibitors versus placebo or usual care, were selected. The primary outcomes considered were all-cause mortality, myocardial infarction, unstable angina, and adverse events. DATA COLLECTION AND ANALYSIS: Two or more review authors, working independently at each step, selected studies, extracted data, assessed the risk of bias and used GRADE to judge the certainty of evidence. MAIN RESULTS: We included 58 RCTs (22,053 participants; 21,308 analysed), comparing medication efficacy with placebo or usual care. Thirty-four trials focused on primary prevention and 24 on secondary prevention. The interventions included IL-1 RAs (anakinra, canakinumab), IL-6 RA (tocilizumab), TNF-inhibitors (etanercept, infliximab) compared with placebo or usual care. The certainty of evidence was low to very low due to biases and imprecision; all trials had a high risk of bias. Primary prevention: IL-1 RAs The evidence is very uncertain about the effects of the intervention on all-cause mortality(RR 0.33, 95% CI 0.01 to 7.58, 1 trial), myocardial infarction (RR 0.71, 95% CI 0.04 to 12.48, I² = 39%, 2 trials), unstable angina (RR 0.24, 95% CI 0.03 to 2.11, I² = 0%, 2 trials), stroke (RR 2.42, 95% CI 0.12 to 50.15; 1 trial), adverse events (RR 0.85, 95% CI 0.59 to 1.22, I² = 54%, 3 trials), or infection (rate ratio 0.84, 95% 0.55 to 1.29, I² = 0%, 4 trials). Evidence is very uncertain about whether anakinra and cankinumab may reduce heart failure (RR 0.21, 95% CI 0.05 to 0.94, I² = 0%, 3 trials). Peripheral vascular disease (PVD) was not reported as an outcome. IL-6 RAs The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 0.68, 95% CI 0.12 to 3.74, I² = 30%, 3 trials), myocardial infarction (RR 0.27, 95% CI 0.04 to1.68, I² = 0%, 3 trials), heart failure (RR 1.02, 95% CI 0.11 to 9.63, I² = 0%, 2 trials), PVD (RR 2.94, 95% CI 0.12 to 71.47, 1 trial), stroke (RR 0.34, 95% CI 0.01 to 8.14, 1 trial), or any infection (rate ratio 1.10, 95% CI: 0.88 to 1.37, I2 = 18%, 5 trials). Adverse events may increase (RR 1.13, 95% CI 1.04 to 1.23, I² = 33%, 5 trials). No trial assessed unstable angina. TNF inhibitors The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 1.78, 95% CI 0.63 to 4.99, I² = 10%, 3 trials), myocardial infarction (RR 2.61, 95% CI 0.11 to 62.26, 1 trial), stroke (RR 0.46, 95% CI 0.08 to 2.80, I² = 0%; 3 trials), heart failure (RR 0.85, 95% CI 0.06 to 12.76, 1 trial). Adverse events may increase (RR 1.13, 95% CI 1.01 to 1.25, I² = 51%, 13 trials). No trial assessed unstable angina or PVD. Secondary prevention: IL-1 RAs The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 0.94, 95% CI 0.84 to 1.06, I² = 0%, 8 trials), unstable angina (RR 0.88, 95% CI 0.65 to 1.19, I² = 0%, 3 trials), PVD (RR 0.85, 95% CI 0.19 to 3.73, I² = 38%, 3 trials), stroke (RR 0.94, 95% CI 0.74 to 1.2, I² = 0%; 7 trials), heart failure (RR 0.91, 95% 0.5 to 1.65, I² = 0%; 7 trials), or adverse events (RR 0.92, 95% CI 0.78 to 1.09, I² = 3%, 4 trials). There may be little to no difference between the groups in myocardial infarction (RR 0.88, 95% CI 0.0.75 to 1.04, I² = 0%, 6 trials). IL6-RAs The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 1.09, 95% CI 0.61 to 1.96, I² = 0%, 2 trials), myocardial infarction (RR 0.46, 95% CI 0.07 to 3.04, I² = 45%, 3 trials), unstable angina (RR 0.33, 95% CI 0.01 to 8.02, 1 trial), stroke (RR 1.03, 95% CI 0.07 to 16.25, 1 trial), adverse events (RR 0.89, 95% CI 0.76 to 1.05, I² = 0%, 2 trials), or any infection (rate ratio 0.66, 95% CI 0.32 to 1.36, I² = 0%, 4 trials). No trial assessed PVD or heart failure. TNF inhibitors The evidence is very uncertain about the effect of the intervention on all-cause mortality (RR 1.16, 95% CI 0.69 to 1.95, I² = 47%, 5 trials), heart failure (RR 0.92, 95% 0.75 to 1.14, I² = 0%, 4 trials), or adverse events (RR 1.15, 95% CI 0.84 to 1.56, I² = 32%, 2 trials). No trial assessed myocardial infarction, unstable angina, PVD or stroke. Adverse events may be underestimated and benefits inflated due to inadequate reporting. AUTHORS' CONCLUSIONS: This Cochrane review assessed the benefits and harms of using interleukin-receptor antagonists and tumour necrosis factor inhibitors for primary and secondary prevention of atherosclerotic diseases compared with placebo or usual care. However, the evidence for the predetermined outcomes was deemed low or very low certainty, so there is still a need to determine whether these interventions provide clinical benefits or cause harm from this perspective. In summary, the different biases and imprecision in the included studies limit their external validity and represent a limitation to determining the effectiveness of the intervention for both primary and secondary prevention of ACVD.

• MeSH
• ateroskleróza * prevence a kontrola   mortalita   MeSH
• humanizované monoklonální protilátky * aplikace a dávkování   škodlivé účinky   MeSH
• infarkt myokardu * prevence a kontrola   mortalita   MeSH
• lidé MeSH
• nestabilní angina pectoris prevence a kontrola   mortalita   MeSH
• příčina smrti MeSH
• primární prevence * metody   MeSH
• randomizované kontrolované studie jako téma MeSH
• receptory interleukinu-1 * antagonisté a inhibitory   MeSH
• sekundární prevence * metody   MeSH
• TNF-alfa * antagonisté a inhibitory   MeSH
• zkreslení výsledků (epidemiologie) MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• metaanalýza MeSH
• systematický přehled MeSH
• Názvy látek
• canakinumab MeSH Prohlížeč
• humanizované monoklonální protilátky * MeSH
• receptory interleukinu-1 * MeSH
• TNF-alfa * MeSH
• tocilizumab MeSH Prohlížeč

Pericardial fluid (PF) has been suggested as a reservoir of molecular targets that can be modulated for efficient repair after myocardial infarction (MI). Here, we set out to address the content of this biofluid after MI, namely in terms of microRNAs (miRs) that are important modulators of the cardiac pathological response. PF was collected during coronary artery bypass grafting (CABG) from two MI cohorts, patients with non-ST-segment elevation MI (NSTEMI) and patients with ST-segment elevation MI (STEMI), and a control group composed of patients with stable angina and without previous history of MI. The PF miR content was analyzed by small RNA sequencing, and its biological effect was assessed on human cardiac fibroblasts. PF accumulates fibrotic and inflammatory molecules in STEMI patients, namely causing the soluble suppression of tumorigenicity 2 (ST-2), which inversely correlates with the left ventricle ejection fraction. Although the PF of the three patient groups induce similar levels of fibroblast-to-myofibroblast activation in vitro, RNA sequencing revealed that PF from STEMI patients is particularly enriched not only in pro-fibrotic miRs but also anti-fibrotic miRs. Among those, miR-22-3p was herein found to inhibit TGF-β-induced human cardiac fibroblast activation in vitro. PF constitutes an attractive source for screening diagnostic/prognostic miRs and for unveiling novel therapeutic targets in cardiac fibrosis.

• Klíčová slova
• cardiac fibroblasts, fibrosis, miR-22-3p, miRNAs, myocardial infarction, pericardial fluid,
• MeSH
• fibroblasty metabolismus   MeSH
• fibróza * MeSH
• infarkt myokardu s elevacemi ST úseků metabolismus   patologie   genetika   MeSH
• infarkt myokardu * metabolismus   genetika   patologie   MeSH
• interleukin-1 receptor-like 1 protein metabolismus   genetika   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mikro RNA * genetika   metabolismus   MeSH
• myokard metabolismus   patologie   MeSH
• perikardiální tekutina * metabolismus   MeSH
• senioři MeSH
• transformující růstový faktor beta metabolismus   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• IL1RL1 protein, human MeSH Prohlížeč
• interleukin-1 receptor-like 1 protein MeSH
• mikro RNA * MeSH
• MIRN22 microRNA, human MeSH Prohlížeč
• transformující růstový faktor beta MeSH

BACKGROUND: Right ventricular pacing (RVP) can result in pacing-induced cardiomyopathy (PICM). It is unknown whether specific biomarkers reflect differences between His bundle pacing (HBP) and RVP and predict a decrease in left ventricular function during RVP. AIMS: We aimed to compare the effect of HBP and RVP on the left ventricular ejection fraction (LVEF) and to study how they affect serum markers of collagen metabolism. METHODS: Ninety-two high-risk PICM patients were randomized to HBP or RVP groups. Their clinical characteristics, echocardiography, and serum levels of transforming growth factor β1 (TGF-β1), matrix metalloproteinase 9 (MMP-9), suppression of tumorigenicity 2 interleukin (ST2-IL), tissue inhibitor of metalloproteinase 1 (TIMP-1), and galectin 3 (Gal-3) were studied before pacemaker implantation and six months later. RESULTS: Fifty-three patients were randomized to the HBP group and 39 patients to the RVP group. HBP failed in 10 patients, who crossed over to the RVP group. Patients with RVP had significantly lower LVEF compared to HBP patients after six months of pacing (-5% and -4% in as-treated and intention-to-treat analysis, respectively). Levels of TGF-β1 after 6 months were lower in HBP than RVP patients (mean difference -6 ng/ml; P = 0.009) and preimplant Gal-3 and ST2-IL levels were higher in RVP patients, with a decline in LVEF ≥5% compared to those with a decline of <5% (mean difference 3 ng/ml and 8 ng/ml; P = 0.02 for both groups). CONCLUSION: In high-risk PICM patients, HBP was superior to RVP in providing more physiological ventricular function, as reflected by higher LVEF and lower levels of TGF-β1. In RVP patients, LVEF declined more in those with higher baseline Gal-3 and ST2-IL levels than in those with lower levels.

• Klíčová slova
• His bundle pacing, markers of collagen metabolism, right ventricular pacing,
• MeSH
• biologické markery MeSH
• elektrokardiografie MeSH
• funkce levé komory srdeční * fyziologie   MeSH
• Hisův svazek MeSH
• interleukin-1 receptor-like 1 protein MeSH
• kardiomyopatie * MeSH
• kardiostimulace umělá škodlivé účinky   MeSH
• kolagen MeSH
• lidé MeSH
• tepový objem fyziologie   MeSH
• tkáňový inhibitor metaloproteinasy 1 MeSH
• transformující růstový faktor beta1 MeSH
• výsledek terapie MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• randomizované kontrolované studie MeSH
• Názvy látek
• biologické markery MeSH
• interleukin-1 receptor-like 1 protein MeSH
• kolagen MeSH
• tkáňový inhibitor metaloproteinasy 1 MeSH
• transformující růstový faktor beta1 MeSH

Obesity is an epidemic condition linked to cardiovascular disease severity and mortality. Fat localization and type represent cardiovascular risk estimators. Importantly, visceral fat secretes adipokines known to promote low-grade inflammation that, in turn, modulate its secretome and cardiac metabolism. In this regard, IL-33 regulates the functions of various immune cells through ST2 binding and-following its role as an immune sensor to infection and stress-is involved in the pro-fibrotic remodeling of the myocardium. Here we further investigated the IL-33/ST2 effects on cardiac remodeling in obesity, focusing on molecular pathways linking adipose-derived IL-33 to the development of fibrosis or hypertrophy. We analyzed the Zucker Fatty rat model, and we developed in vitro models to mimic the adipose and myocardial relationship. We demonstrated a dysregulation of IL-33/ST2 signaling in both adipose and cardiac tissue, where they affected Epac proteins and myocardial gene expression, linked to pro-fibrotic signatures. In Zucker rats, pro-fibrotic effects were counteracted by ghrelin-induced IL-33 secretion, whose release influenced transcription factor expression and ST2 isoforms balance regulation. Finally, the effect of IL-33 signaling is dependent on several factors, such as cell types' origin and the balancing of ST2 isoforms. Noteworthy, it is reasonable to state that considering IL-33 to have a unique protective role should be considered over-simplistic.

• Klíčová slova
• 3/10 max, IL-33/ST2, adipose tissue, cardiac remodeling, cardiovascular disease, obesity,
• MeSH
• fibróza genetika   metabolismus   MeSH
• ghrelin genetika   metabolismus   MeSH
• interleukin 33 * genetika   metabolismus   MeSH
• interleukin-1 receptor-like 1 protein genetika   metabolismus   MeSH
• kardiomegalie genetika   metabolismus   MeSH
• krysa rodu Rattus MeSH
• modely nemocí na zvířatech MeSH
• myokard metabolismus   MeSH
• obezita * komplikace   genetika   metabolismus   MeSH
• potkani Zucker MeSH
• receptory interleukinu-1 * genetika   metabolismus   MeSH
• remodelace komor * genetika   fyziologie   MeSH
• výměnné faktory guaninnukleotidů genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• ghrelin MeSH
• Il33 protein, rat MeSH Prohlížeč
• interleukin 33 * MeSH
• interleukin-1 receptor-like 1 protein MeSH
• obestatin, rat MeSH Prohlížeč
• Rapgef3 protein, rat MeSH Prohlížeč
• receptory interleukinu-1 * MeSH
• ST2 protein, rat MeSH Prohlížeč
• výměnné faktory guaninnukleotidů MeSH

Optimization of therapy of cerebrovascular disorders (CVD) is one of the most critical health problems. The current treatment regimen of CVD turns out to be often insufficient. Search for new drugs with cerebroprotective and antihypoxic properties is an essential task of modern medicine and pharmacy. Attention to cytokine mechanisms of ischemic brain damage in clinics and experimental research has been increased recently. Interleukin-1 (IL-1) receptor blockade is a perspective way of cerebroprotection that requires a more profound study of its mechanisms. The article contains the results of a study of cerebroprotective and antihypoxic properties of the recombinant IL-1 antagonist raleukin on a model of bilateral carotid occlusion in rats. Recombinant receptor antagonist IL-1 raleukin (15 mg/kg) did not affect basal blood flow in the internal carotid artery of intact group animals. Still, it prevented its decrease approximately three times in case of occlusion of both common carotid arteries followed by reperfusion. Indicators of the cerebroprotective effect of studied medication were reducing the acidotic blood shift flowing from the brain of animals with irreversible bilateral carotid occlusion, neuronal degradation, and weakening.

• Klíčová slova
• Cerebral ischemia, bilateral carotid occlusion, interleukin-1, neuron-specific enolase, raleukin,
• MeSH
• interleukin-1 metabolismus   farmakologie   MeSH
• kardiovaskulární nemoci * MeSH
• krysa rodu Rattus MeSH
• mozek * krevní zásobení   metabolismus   MeSH
• receptory interleukinu-1 metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• interleukin-1 MeSH
• receptory interleukinu-1 MeSH

BACKGROUND: Circulating markers are attractive molecules for prognosis and management of cancer that allow sequential monitoring of patients during and after treatment. Based on previous protein profiling data, circulating interleukin 1 receptor antagonist (IL-1Ra) was evaluated as a potential diagnostic and prognostic marker for squamous cell carcinomas of the head and neck (SCCHN). In this study, we aimed at confirming the clinical relevance of plasma IL-1Ra in SCCHN and exploring its potential as a prediction marker for SCCHN. METHODS: Plasma from 87 patients with SCCHN, control plasma from 28 healthy individuals and pre-diagnostic plasma from 44 patients with squamous cell carcinoma of the oral tongue (SCCOT) and 88 matched controls were analysed with IL-1Ra electrochemiluminescence immunoassays from mesoscale diagnostics. RESULTS: Plasma IL-1Ra was found to be up-regulated in patients with oral tongue, gingiva and base of tongue tumours compared to healthy individuals (p < 0.01). IL-1Ra levels positively correlated with tumour size (p < 0.01) and body mass index (p = 0.013). Comparing pre-diagnostic plasma to the matched controls, similar IL1-Ra levels were seen (p = 0.05). CONCLUSION: The anti-inflammatory cytokine IL-1Ra could be a diagnostic marker for SCCHN, whereas its potential as a cancer prediction marker was not supported by our data.

• Klíčová slova
• IL-1Ra, plasma, squamous cell carcinoma,
• MeSH
• antagonista receptoru pro interleukin 1 MeSH
• dlaždicobuněčné karcinomy hlavy a krku MeSH
• lidé MeSH
• nádory hlavy a krku * MeSH
• receptory interleukinu-1 MeSH
• spinocelulární karcinom * diagnóza   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antagonista receptoru pro interleukin 1 MeSH
• receptory interleukinu-1 MeSH

We find that cardiac group 2 innate lymphoid cells (ILC2s) are essential for the development of IL-33-induced eosinophilic pericarditis. We show a pathogenic role for ILC2s in cardiac inflammation, in which ILC2s activated by IL-33 drive the development of eosinophilic pericarditis in collaboration with cardiac fibroblasts. ILCs, not T and B cells, are required for the development of pericarditis. ILC2s transferred to the heart of Rag2-/-Il2rg-/- mice restore their susceptibility to eosinophil infiltration. Moreover, ILC2s direct cardiac fibroblasts to produce eotaxin-1. We also find that eosinophils reside in the mediastinal cavity and that eosinophils transferred to the mediastinal cavity of eosinophil-deficient ΔdblGATA1 mice following IL-33 treatment migrate to the heart. Thus, the serous cavities may serve as a reservoir of cardiac-infiltrating eosinophils. In humans, patients with pericarditis show higher amounts of ILCs in pericardial fluid than do healthy controls and patients with other cardiac diseases. We demonstrate that ILCs play a critical role in pericarditis.

• Klíčová slova
• IL-33, Innate lymphoid cells, cardiac inflammation, eosinophils, group 2 innate lymphoid cells, mediastinum, pericarditis, serosal cavity,
• MeSH
• chemokin CCL11 genetika   metabolismus   MeSH
• eozinofily účinky léků   patologie   MeSH
• fibroblasty účinky léků   metabolismus   MeSH
• funkční vyšetření srdce účinky léků   MeSH
• interleukin 33 farmakologie   MeSH
• interleukin-1 receptor-like 1 protein nedostatek   metabolismus   MeSH
• interleukin-5 metabolismus   MeSH
• lidé MeSH
• lymfocyty účinky léků   imunologie   MeSH
• mediastinum patologie   MeSH
• myši inbrední BALB C MeSH
• náchylnost k nemoci MeSH
• perikarditida genetika   imunologie   patofyziologie   MeSH
• pohyb buněk účinky léků   MeSH
• přirozená imunita * účinky léků   MeSH
• regulace genové exprese účinky léků   MeSH
• signální transdukce účinky léků   MeSH
• srdce účinky léků   patofyziologie   MeSH
• upregulace účinky léků   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• chemokin CCL11 MeSH
• Il1rl1 protein, mouse MeSH Prohlížeč
• interleukin 33 MeSH
• interleukin-1 receptor-like 1 protein MeSH
• interleukin-5 MeSH

Overactivation of the innate immune system together with the impaired downstream pathway of type I interferon-responding genes is a hallmark of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc). To date, limited data on the cross-disease innate gene signature exists among those diseases. We compared therefore an innate gene signature of Toll-like receptors (TLRs), seven key members of the interleukin (IL)1/IL1R family, and CXCL8/IL8 in peripheral blood mononuclear cells from well-defined patients with active stages of RA (n = 36, DAS28 ≥ 3.2), SLE (n = 28, SLEDAI > 6), and SSc (n = 22, revised EUSTAR index > 2.25). Emerging diversity and abundance of the innate signature in RA patients were detected: RA was characterized by the upregulation of TLR3, TLR5, IL1RAP/IL1R3, IL18R1, and SIGIRR/IL1R8 when compared to SSc (P corr < 0.02) and of TLR2, TLR5, and SIGIRR/IL1R8 when compared to SLE (P corr < 0.02). Applying the association rule analysis, six rules (combinations and expression of genes describing disease) were identified for RA (most frequently included high TLR3 and/or IL1RAP/IL1R3) and three rules for SLE (low IL1RN and IL18R1) and SSc (low TLR5 and IL18R1). This first cross-disease study identified emerging heterogeneity in the innate signature of RA patients with many upregulated innate genes compared to that of SLE and SSc.

• MeSH
• dospělí MeSH
• interleukin-1 genetika   metabolismus   MeSH
• interleukin-8 genetika   metabolismus   MeSH
• leukocyty mononukleární metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• přirozená imunita genetika   MeSH
• receptory interleukinu-1 - typ I genetika   metabolismus   MeSH
• revmatoidní artritida krev   genetika   imunologie   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• systémová sklerodermie krev   genetika   imunologie   MeSH
• systémový lupus erythematodes krev   genetika   imunologie   MeSH
• toll-like receptory genetika   metabolismus   MeSH
• transkriptom MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• interleukin-1 MeSH
• interleukin-8 MeSH
• receptory interleukinu-1 - typ I MeSH
• toll-like receptory MeSH

Background Myocarditis is an important cause of acute and chronic heart failure. Men with myocarditis have worse recovery and an increased need for transplantation compared with women, but the reason for the sex difference remains unclear. Elevated sera soluble (s) ST2 predicts mortality from acute and chronic heart failure, but has not been studied in myocarditis patients. Methods and Results Adults with a diagnosis of clinically suspected myocarditis (n=303, 78% male) were identified according to the 2013 European Society of Cardiology position statement. Sera sST2 levels were examined by ELISA in humans and mice and correlated with heart function according to sex and age. Sera sST2 levels were higher in healthy men ( P=8×10-6) and men with myocarditis ( P=0.004) compared with women. sST2 levels were elevated in patients with myocarditis and New York Heart Association class III - IV heart failure ( P=0.002), predominantly in men ( P=0.0003). Sera sST2 levels were associated with New York Heart Association class in men with myocarditis who were ≤50 years old ( r=0.231, P=0.0006), but not in women ( r=0.172, P=0.57). Sera sST2 levels were also significantly higher in male mice with myocarditis ( P=0.005) where levels were associated with cardiac inflammation. Gonadectomy with hormone replacement showed that testosterone ( P<0.001), but not estradiol ( P=0.32), increased sera sST2 levels in male mice with myocarditis. Conclusions We show in a well-characterized subset of heart failure patients with clinically suspected and biopsy-confirmed myocarditis that elevated sera sST2 is associated with an increased risk of heart failure based on New York Heart Association class in men ≤50 years old.

• Klíčová slova
• biomarkers, heart failure, myocarditis, sST2, sex differences,
• MeSH
• biologické markery krev   MeSH
• biopsie MeSH
• dospělí MeSH
• ELISA MeSH
• interleukin-1 receptor-like 1 protein krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• myokard patologie   MeSH
• myokarditida krev   komplikace   diagnóza   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• následné studie MeSH
• prognóza MeSH
• retrospektivní studie MeSH
• sexuální faktory MeSH
• srdeční selhání krev   diagnóza   etiologie   MeSH
• věkové faktory MeSH
• zvířata MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• multicentrická studie MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• srovnávací studie MeSH
• Názvy látek
• biologické markery MeSH
• IL1RL1 protein, human MeSH Prohlížeč
• interleukin-1 receptor-like 1 protein MeSH

Heart failure (HF) is a complex clinical syndrome which is manifested by characteristic symptoms and objective signs of cardiac insufficiency. The incidence of HF, particularly its chronic form, is estimated 0.4-2 % in the central and western Europe, with an increase in higher age groups, affecting 10-20 % of the population aged over 80. With respect to its growing incidence and prevalence, novel modalities of pharmacological and non-pharmacological treatment are being developed in order to improve quality of life and survival of the affected patients. This review based on up-to-date guidelines focuses in the first part on brief description of the possibilities of diagnosing heart failure, including the novelties arising out from the latest clinical and preclinical studies (such as soluble ST2, FSTL1, etc), further it concentrates on innovations in pharmacological treatment of chronic (ivabradine, ARNI, gliflozins) and acute (ularitide, serelaxin, nesiritide) HF. The last part provides an overview of available non-pharmacological HF therapeutics options (modulation of cardiac contraction, influencing the activity of sympathetic and parasympathetic nervous systems and permanent and temporary device support).Key words: ARNI - ECMO - gliflozins - heart failure - modulation of sympathetic and parasympathetic nervous systems - sacubitril-valsartan - therapy.

• MeSH
• akutní nemoc MeSH
• aminobutyráty terapeutické užití   MeSH
• antagonisté receptorů pro angiotenzin terapeutické užití   MeSH
• atriální natriuretický faktor terapeutické užití   MeSH
• benzazepiny terapeutické užití   MeSH
• bifenylové sloučeniny MeSH
• chronická nemoc MeSH
• diuretika terapeutické užití   MeSH
• fixní kombinace léků MeSH
• interleukin-1 receptor-like 1 protein krev   MeSH
• ivabradin MeSH
• kardiovaskulární látky terapeutické užití   MeSH
• kvalita života MeSH
• lidé MeSH
• natriuretické látky terapeutické užití   MeSH
• natriuretický peptid typu B terapeutické užití   MeSH
• peptidové fragmenty terapeutické užití   MeSH
• proteiny související s folistatinem krev   MeSH
• rekombinantní proteiny terapeutické užití   MeSH
• relaxin terapeutické užití   MeSH
• srdeční selhání krev   diagnóza   farmakoterapie   MeSH
• tetrazoly terapeutické užití   MeSH
• valsartan MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Geografické názvy
• Evropa MeSH
• Názvy látek
• aminobutyráty MeSH
• antagonisté receptorů pro angiotenzin MeSH
• atriální natriuretický faktor MeSH
• benzazepiny MeSH
• bifenylové sloučeniny MeSH
• diuretika MeSH
• fixní kombinace léků MeSH
• FSTL1 protein, human MeSH Prohlížeč
• IL1RL1 protein, human MeSH Prohlížeč
• interleukin-1 receptor-like 1 protein MeSH
• ivabradin MeSH
• kardiovaskulární látky MeSH
• natriuretické látky MeSH
• natriuretický peptid typu B MeSH
• peptidové fragmenty MeSH
• proteiny související s folistatinem MeSH
• rekombinantní proteiny MeSH
• relaxin MeSH
• sacubitril and valsartan sodium hydrate drug combination MeSH Prohlížeč
• serelaxin protein, human MeSH Prohlížeč
• tetrazoly MeSH
• Ularitide MeSH Prohlížeč
• valsartan MeSH